Stephen B. Hanauer, MD


February 09, 2016

Seeking Clarity on Causation

Recently, I chaired two important meetings with relevant updates and advances in inflammatory bowel disease (IBD): the annual meeting of the American College of Gastroenterology (ACG), held October 16-21 in Honolulu, Hawaii, and Advances in Inflammatory Bowel Diseases (AIBD), December 10-12 in Orlando, Florida. As outgoing president of ACG and ongoing co-chair of AIBD, I was immersed in both programs and would like to summarize some of my observations.

One thing that is clear is that we are making more progress from the standpoint of disease management than we are regarding disease causation. Current research paradigms continue to focus on interactions between genetics and environmental factors.[1] It does not appear that either alone are sufficient causative factors—although in very early-onset IBD in children, the earlier the emergence of the disease, the greater the genetic contribution.

However, as the incidence and prevalence of IBD spreads from the Western world to Asia, there is a discordance of gene mutations associated with ulcerative colitis and Crohn disease despite similarities in phenotypes and disease behavior. As immigrants from second- and third-world environments move to the West or adopt Western lifestyles, the incidence of IBD increases. Whether this is related to hygiene or diet, there is probably an impact on the enterobiome, which now must be expanded beyond the microbiome to include viral and fungal species.

The key finding thus far related to the microbiome is that microbial diversity is reduced in the setting of active IBD. Whether this should be considered a chicken or egg remains to be determined, but acknowledging that diversity is a promising sign of the times.

IBD Management Controversies

One of the controversies regarding disease management derives from the recent SCENIC consensus statement, which recommends chromoendoscopy for dysplasia in ulcerative colitis owing to its increased sensitivity.[2]

Although this consensus was endorsed by the American Gastroenterological Association and American Society for Gastrointestinal Endoscopy, the ACG did not endorse it—and, indeed, neither of the endorsing societies elevated the consensus to "guideline" status. The discourse in the SCENIC document and accompanying editorial by Marion and Sands[3] provide details on methodologies to detect dysplasia and cancer in ulcerative colitis.

One might summarize the controversies by accepting that the closer and harder one looks, the more dysplasia one will identify. The question is not one of sensitivity, but of specificity. Although more low-grade dysplastic lesions are identified using chromoendoscopy, no data indicate that it reduces the risk of developing cancer more than careful high-definition white-light exams. Few gastroenterologists are performing "routine" chromoendoscopy on every ulcerative colitis surveillance examination,[4] and the risk of developing cancer in patients who undergo "surveillance of any kind" has been greatly reduced to essentially the same as that in the general population.[5]

There is little controversy regarding the role of chromoendoscopy to clarify the boundaries of lesions, to follow up on dysplasia identified in nontargeted biopsies, or to better examine patients with prior lesions or numerous pseudopolyps. Another general consensus is that the value of blind, nontargeted biopsies is very limited.[2]


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